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Cephalic Phase Insulin Response: Can we get fat without excess nutrient intake?

A rather obscure physiological phenomena that people are unfamiliar with is called the cephalic-phase insulin response (abbreviated: CPIR from hereon). You may have been acquainted with this theory if you've read Kiefer's Carb Backloading eBook as he has a view excerpts therein that discuss this process.

Essentially, this phenomena could present a physiological basis for how individuals do indeed stimulate a tendency to store free fatty acids in the absence of nutrient absorption. Why is this of concern? Well, if you're one who consumes a lot of "non-nutritive/low-calorie" sweeteners and/or beverages, you could in fact be hindering your fat loss efforts by constantly secreting insulin around the clock and blunting your ability to burn adipose tissue, DESPITE being in a caloric deficit.

So what exactly is this CPIR we speak of? Well, in a nutshell, it's a mechanism initiated in the pre-absorptive phase of feeding. You're likely familiar that with the ingestion of sweet/starchy foods we secrete insulin from pancreatic beta cells which work to upregulate GLUT transport proteins in body tissues (and thus shuttle nutrients into the cell).

Where the CPIR differs from the fed state release of insulin is that this actually occurs before nutrients have actually been ingested at all. For example, the CPIR is proposed to happen simply by "sensing" you are preparing to eat something starchy/sweet, thus prepping the body for storing nutrients (via secretion of insulin). So a real-world example of this would be coming home and smelling mama's sweet cookies popping out of the oven as you hobble over to the kitchen, salivating over your accompanying glass of warm milk.

Naturally, the rebuttle to this would be, well then aren't people who work in a food/restaurant environment being constantly predisposed to this sensory stimulation? Honestly, at this point in time I can't answer yes or no to that question, but what I can propose is that the CPIR is a consciously-stimulated phenomena.

What do I mean by this? Well, if you're working in a food/restaurant environment, you likely are not consciously aware of the aroma of food at every waking moment, and in fact once you've been in that environment long enough you've probably adapted to it unconsciously.

Moreover, the CPIR includes other sensory pathways such as sight and not surprisingly taste (e.g. drinking something sweet but non-nutritive like diet soda). However, I have little reason to believe that touch and sound have much to do with the CPIR since we generally don't associate these senses with the ingestion of food.

Too keep this post from getting too convoluted, I will quickly cover the proposed mechanism behind how this actually stimulates adipogenesis depsite the absence of nutrient intake. As of now, it appears that the CPIR concurrently increases the propensity of an enzyme called lipoprotein lipase preferentially in adipose tissue.

So why is this of concern? Well this enzyme is responsible for metabolism/hydrolysis of triglycerides in vivo. Lipoproteins transport fat from the intestines to the bloodstream, where the fat is converted into energy or stored. Thus, if a deficiency of lipoprotein lipase exists, fatty deposits might accumulate in the blood, which could lead to atherosclerosis and obesity.

But what many studies have found is that the response of LPL is actually tissue specific. Optimally, we would want a low expression of LPL in adipose tissue and an elevated expression of it in muscle. Much to our chagrin, at this point, it appears that the CPIR does the inverse of this, and thus can cause excess fatty acid deposition in adipose tissue and promote obesity.

I will leave it at this for now since this is a new concept to many people and I'm sure many questions are already stirring in your head, especially if you're one who loves Splenda, Stevia, diet pop, etc. I'm actually a big user of non-nutritive sweeteners during my fasting period but some of these findings may in fact swing me to reconsider using them during my fasting period (and Kiefer actually reasoned this in his book as well).

I have read that the body responds to the taste of sweetness, even from non-sugar sources, in the same way it responds to carbs; they've even trialled this further and had sports people swill sweet tasting drinks around the mouth and spit them out, only to show that the brain and body still respond by seeing it as ingested carb and therefore energy.

It's intriguing, though I'm not sure I'd agree with either just visual or aroma causing the same responses.

I have read that the body responds to the taste of sweetness, even from non-sugar sources, in the same way it responds to carbs; they've even trialled this further and had sports people swill sweet tasting drinks around the mouth and spit them out, only to show that the brain and body still respond by seeing it as ingested carb and therefore energy.

It's intriguing, though I'm not sure I'd agree with either just visual or aroma causing the same responses.

Yep, thats essentially what the CPIR is. I still hypothesize that its mediated by a conscious sensing of impending sweetness/starch intake that causes the CPIR. It makes sense physiologically that the body would secrete insulin in circumstances when it's preparing for carbohydrate ingestion.

I don't know enough about the physiology of insulin to comment directly on the findings. However, in general I would have two issues:

1) It sounds like it's relegating calories in vs calories out to a subsidiary role in fat loss. To my knowledge, whenever calorie expenditure and intake have been carefully monitored under lab conditions, everyone who experiences a sustained calorie deficit reliably loses fat. There's also a wealth of evidence to suggest that in the real world people are really poor at (a) compliance with nutritional programs (b) estimating their calorific intake and (c) estimating their energy expenditure. Taking these two things together, it supports the idea that calorie deficit really is king. Where it doesn't seem to be working is mainly because they're over-estimating calories in or under-estimating calories out.

2) It falls into the general category of 'blame substance X'. In this case, artificial sweeteners. I'll admit this isn't a scientific objection. Just an observation that there is often a tendency in internet discussions of nutrition to try to identify the villain of the piece (although in some cases, I don't think there's much argument: there's a lot of science behind the vilification of trans-fats, for example). Other arguments have been made for gluten, MSG, 'nightshade foods', fructose and so on and so on.

You mention Kiefer's ideas. I don't necessarily dismiss the research of guys like Kiefer, and he certainy knows a thousand times more about nutrition than me. But I think it's worth remembering he does make money from an ebook promoting nutrient timing as the key to fat loss. Whereas if his ebook said Consume less calories than you expend. Do some weights to preserve lean body mass. That's it. then no one would buy it.

Yep, thats essentially what the CPIR is. I still hypothesize that its mediated by a conscious sensing of impending sweetness/starch intake that causes the CPIR. It makes sense physiologically that the body would secrete insulin in circumstances when it's preparing for carbohydrate ingestion.

That sounds absolutely plausible to me. After all, I can make my mouth water now just by thinking about a roast dinner. So there's a link from higher brain centres to salivary glands to start producing amylase in anticipation of those lovely roast potatoes Why not insulin too?

My only response is that, this so called phenomenon doesn't effect everyone in the same manner when a calorie deficit is present. With experience as my personal teacher, I bet I could consume simple sugar every hour on the hour, consume diet soda with splenda or other artificial sweetener every hour on the hour or another simular beverage, and lose tissue, and most notably fat tissue..in a large calorie deficit...... despite the insulin response. Not wise... But is in fact possible.

Insulin while a storage and removal hormone, is also a multitasking hormone (like shuttling nutrients in and out, etc, etc), and there are many hormones that are involved in removal and deposit of fat tissue in conjunction with insulin, and not insulin alone. Though it is a major player, of course, but it's not the only one.

I don't know enough about the physiology of insulin to comment directly on the findings. However, in general I would have two issues:

1) It sounds like it's relegating calories in vs calories out to a subsidiary role in fat loss. To my knowledge, whenever calorie expenditure and intake have been carefully monitored under lab conditions, everyone who experiences a sustained calorie deficit reliably loses fat. There's also a wealth of evidence to suggest that in the real world people are really poor at (a) compliance with nutritional programs (b) estimating their calorific intake and (c) estimating their energy expenditure. Taking these two things together, it supports the idea that calorie deficit really is king. Where it doesn't seem to be working is mainly because they're over-estimating calories in or under-estimating calories out.

2) It falls into the general category of 'blame substance X'. In this case, artificial sweeteners. I'll admit this isn't a scientific objection. Just an observation that there is often a tendency in internet discussions of nutrition to try to identify the villain of the piece (although in some cases, I don't think there's much argument: there's a lot of science behind the vilification of trans-fats, for example). Other arguments have been made for gluten, MSG, 'nightshade foods', fructose and so on and so on.

You mention Kiefer's ideas. I don't necessarily dismiss the research of guys like Kiefer, and he certainy knows a thousand times more about nutrition than me. But I think it's worth remembering he does make money from an ebook promoting nutrient timing as the key to fat loss. Whereas if his ebook said Consume less calories than you expend. Do some weights to preserve lean body mass. That's it. then no one would buy it.

You bring up some good points to consider here Tannhauser. The mechanism for how the CPIR can potentially cause fatty acid deposition independent of nutrient intake is still rather misunderstood (at least from the studies I've read).

It's also important to consider the physiology of how weight gain occurs as a whole (or rather, via nutrient-dependent pathways). In the case of energy excess, we are specifically looking at a state of high ATP:ADP ratio in the cell, which thus downregulates AMPk phosphorylation and shuts off fat-burning. Insulin is a also an inhibitor of AMPk so it is possible that the cell is sensing a "pseudo" excess in energy in this case. Granted Im merely speaking extemporaneously here and just trying to stimulate possible mechanisms for how the CPIR could induce fat gain.

Quote:

Originally Posted by Tannhauser

That sounds absolutely plausible to me. After all, I can make my mouth water now just by thinking about a roast dinner. So there's a link from higher brain centres to salivary glands to start producing amylase in anticipation of those lovely roast potatoes Why not insulin too?

Yes, the digestive system pretty much does have pre-absorptive duties such as secretion of gastric juices to prepare for food ingestion.

My only response is that, this so called phenomenon doesn't effect everyone in the same manner when a calorie deficit is present. With experience as my personal teacher, I bet I could consume simple sugar every hour on the hour, consume diet soda with splenda or other artificial sweetener every hour on the hour or another simular beverage, and lose tissue, and most notably fat tissue..in a large calorie deficit...... despite the insulin response. Not wise... But is in fact possible.

Insulin while a storage and removal hormone, is also a multitasking hormone (like shuttling nutrients in and out, etc, etc), and there are many hormones that are involved in removal and deposit of fat tissue in conjunction with insulin, and not insulin alone. Though it is a major player, of course, but it's not the only one.

Peace and happiness,

Don

Hey Don,

Well this brings up the individuality of it all, since some people are naturally highly insulin-sensitive and it won't really effect them one way or the other. Others, especially those predisposed to obesity, are usually already insulin-resistant so it doesn't surprise me that there is more to this topic than just insulin.
I'm actually more intrigued by the role of LPL in this whole schematic. Specifically because LPL has been cited as one of the reasons people who sit all day may be prone to fat storage and inhibited fat burning IN SPITE of caloric expenditure exceeding caloric intake.